Journal
JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY
Volume 27, Issue -, Pages 94-98Publisher
WILEY
DOI: 10.1111/j.1440-1746.2011.07022.x
Keywords
necdin; Ppar gamma; Shh; Wnt
Categories
Funding
- NIAAA NIH HHS [U01 AA018663, R24 AA012885, P50 AA011999, R01 AA018857, R01AA020753, U01AA018663, R24AA12885, P50 AA011999-13, R24 AA012885-11, R01 AA020753, R01AA018857, P50AA11999, U01 AA018663-02] Funding Source: Medline
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Hepatic stellate cells (HSC) are the liver mesenchymal cell type which responds to hepatocellular damage and participates in wound healing. Although HSC myofibroblastic trans-differentiation (activation) is implicated in excessive extracellular matrix deposition, molecular understanding of this phenotypic switch from the viewpoint of cell fate regulation is limited. Recent studies demonstrate the roles of anti-adipogenic morphogens (Wnt, Necdin, Shh) in epigenetic repression of the HSC differentiation gene Ppar gamma as a causal event in HSC activation. These morphogens have positive cross-interactions which converge to epigenetic repression of Ppar gamma involving the methyl-CpG binding protein MeCP2. However, these morphogens expressed by activated HSC may also participate in cross-talk between HSC and hepatoblasts/hepatocytes to support liver regeneration, and their aberrant regulation may contribute to liver tumorigenesis. Implications of HSC-derived morphogens in these possibilities are discussed.
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